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Limited resistance of hypertrophied skeletal muscle to glucocorticoids.
J Steroid Biochem. 1986 Jun; 24(6):1179-83.JS

Abstract

Male hypophysectomized rats were initially assigned to a control or an overloaded group that underwent compensatory hypertrophy of plantaris muscles to steady-state levels following removal of synergistic musculature. Plantaris muscle mass of overloaded animals was higher than that of controls by 38% (391 +/- 8 vs 284 +/- 7 mg) and glucocorticoid cytosol specific binding concentrations, using [3H]triamcinolone acetonide (TA) as the labeled steroid, was also significantly higher in hypertrophied muscles (83.3 +/- 3.9 fmol . mg protein-1) than in control muscles 56.3 +/- 3.9 fmol . mg protein-1). Cortisone acetate (CA) was then administered daily subcutaneously in high, 100 mg; intermediate, 10 mg; or low, 1.0 mg . kg-1 body wt doses. Groups of rats were killed after 1/4, 2 days and 7 days. Absolute muscle mass losses after 7 days of CA treatment were approx 80 mg with high doses and 60 mg with intermediate doses in both hypertrophied and control muscles. The low CA dose did not produce atrophy. The absolute depletion of [3H]TA binding activity with CA treatment was always greater in hypertrophied muscles of high and intermediate dose treated than those of their respective controls, but TA binding capacities remained higher in hypertrophied muscles than in controls at almost all time points in all treatment groups. Unlike previous findings in which the simultaneous initiation of overload prevented glucocorticoid induced muscle wasting, no resistance to the effect of CA treatment was observed when treatment was begun after hypertrophy had occurred.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

3736045

Citation

Hickson, R C., et al. "Limited Resistance of Hypertrophied Skeletal Muscle to Glucocorticoids." Journal of Steroid Biochemistry, vol. 24, no. 6, 1986, pp. 1179-83.
Hickson RC, Galassi TM, Capaccio JA, et al. Limited resistance of hypertrophied skeletal muscle to glucocorticoids. J Steroid Biochem. 1986;24(6):1179-83.
Hickson, R. C., Galassi, T. M., Capaccio, J. A., & Chatterton, R. T. (1986). Limited resistance of hypertrophied skeletal muscle to glucocorticoids. Journal of Steroid Biochemistry, 24(6), 1179-83.
Hickson RC, et al. Limited Resistance of Hypertrophied Skeletal Muscle to Glucocorticoids. J Steroid Biochem. 1986;24(6):1179-83. PubMed PMID: 3736045.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Limited resistance of hypertrophied skeletal muscle to glucocorticoids. AU - Hickson,R C, AU - Galassi,T M, AU - Capaccio,J A, AU - Chatterton,R T,Jr PY - 1986/6/1/pubmed PY - 2001/3/28/medline PY - 1986/6/1/entrez SP - 1179 EP - 83 JF - Journal of steroid biochemistry JO - J. Steroid Biochem. VL - 24 IS - 6 N2 - Male hypophysectomized rats were initially assigned to a control or an overloaded group that underwent compensatory hypertrophy of plantaris muscles to steady-state levels following removal of synergistic musculature. Plantaris muscle mass of overloaded animals was higher than that of controls by 38% (391 +/- 8 vs 284 +/- 7 mg) and glucocorticoid cytosol specific binding concentrations, using [3H]triamcinolone acetonide (TA) as the labeled steroid, was also significantly higher in hypertrophied muscles (83.3 +/- 3.9 fmol . mg protein-1) than in control muscles 56.3 +/- 3.9 fmol . mg protein-1). Cortisone acetate (CA) was then administered daily subcutaneously in high, 100 mg; intermediate, 10 mg; or low, 1.0 mg . kg-1 body wt doses. Groups of rats were killed after 1/4, 2 days and 7 days. Absolute muscle mass losses after 7 days of CA treatment were approx 80 mg with high doses and 60 mg with intermediate doses in both hypertrophied and control muscles. The low CA dose did not produce atrophy. The absolute depletion of [3H]TA binding activity with CA treatment was always greater in hypertrophied muscles of high and intermediate dose treated than those of their respective controls, but TA binding capacities remained higher in hypertrophied muscles than in controls at almost all time points in all treatment groups. Unlike previous findings in which the simultaneous initiation of overload prevented glucocorticoid induced muscle wasting, no resistance to the effect of CA treatment was observed when treatment was begun after hypertrophy had occurred. SN - 0022-4731 UR - https://www.unboundmedicine.com/medline/citation/3736045/Limited_resistance_of_hypertrophied_skeletal_muscle_to_glucocorticoids_ L2 - https://medlineplus.gov/steroids.html DB - PRIME DP - Unbound Medicine ER -